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The most frequent genetic mutations and defects are found in SOD1 (Ghasemi and Brown, 2018), a gene encoding an essential copper/zinc antioxidant enzyme which is likely involved in both familiar and sporadic presentations (Tafuri et al., 2015)

Targeting FIT2, a protein essential for LD formation, the authors demonstrated reducing LD accumulation in brain macrophages could restore their pathological phenotypes in an AD mouse model (Wu et al., 2025)

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Could lipid infusion be a risk for parenteral nutrition-associated cholestasis in low birth weight neonates